Reactive Oxygen Species (ROS) can induce carcinogenesis via DMA injury. Both enzymatic and non-enzymatic antioxidants participate in cell protection against harmful influence of oxidative stress. The aim of the present study was to assess the level of end product of lipid peroxidation such as malondialdehyde (MDA) as an oxidant in colorectal cancer. Moreover, we analyzed the activity of main non-enzymatic antioxidants, vitamin E and vitamin C in colorectal cancer patients. In the present study, total 48 samples were analyzed which includes 24 age matched healthy controls irrespective of sex (Group I) and 24 cases of colorectal cancer (Group II). The serum level of lipid peroxide, vitamin E and vitamin C were estimated in both healthy control Group I (n=24) and colorectal cancer Group II (n=24). A significant increase in the level of serum lipid peroxide (P<0.001), with concomitant decrease in the levels of serum vitamin E and vitamin C, (P<0.001) in Group II patients were noticed as compared to the healthy control Group I. Our findings suggest that increased oxidative stress and reduced antioxidants defense mechanism may play an important role in progression and pathogenesis of colorectal cancer.
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The current theory suggests that in preeclampsia there is an increase in the lipid peroxidation products and leads to a decrease in the plasma antioxidants except uric acid.Along with this change in the lipid profile level leads to the pathogenesis of preeclampsia.In this context, this study was undertaken to determine the changes in plasma levels of lipid peroxide, antioxidant levels in women with preeclampsia and to investigate the effect on lipid profile. To measure the levels of serum lipid profile in preeclampsia in comparison with normal pregnancy. Cross sectional study consisting of 30 preeclamptic and 30 healthy pregnant women. Fasting venous blood samples were collected during antepartum period and plasma levels of TG, TC, HDL-C, VLDL-C, and LDL-C were measured.: In the preeclamptic group, there was a significant increase in the triglyceride levels, but there were no significant changes in other lipid profile parameters. The findings of the present study are consistent with previous studies, lipid profile levels are important factors in the pathogenesis of preeclampsia. In preeclampsia plasma antioxidants are excessively utilized to counteract the cellular changes mediated by free radicals.
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Objective: Lead (Pb) is a long-known poison of environment and industrial origin. Its prolonged exposure affects cellular material and alters cellular genetics and produces oxidative damages. In this study, we investigated the exposure of chronic sustained hypoxia or lead acetate alone or in combination with or without supplementation of α-tocopherol on hepatic oxidative and nitrosative stress in rats. Materials and Methods: The rats weighing 165 ± 5 g were exposed to chronic sustained hypoxia (10% oxygen) or lead acetate (25 mg/kg of body weight, intraperitoneally) alone or in combination with or without supplementation of α-tocopherol (10 mg/100 g b.wt, intramuscularly). The body weight of all the rats was recorded on the day 1 of the treatment and the day of sacrifice. Serum lipid profile was estimated by using a biochemical analyzer. Oxidant and enzymatic antioxidants status was evaluated by using spectrophotometer. Serum levels of hypoxia inducible factor-1 alpha (HIF-1α) and vascular endothelial growth factor (VEGF) were measured by using ELISA technique. Histopathological assessments of hepatic tissue were also done. Results: Exposure of both lead and hypoxia showed decreased body weight, altered serum lipid profile, oxidant and enzymatic antioxidants status, serum HIF-1α and VEGF concentrations. Simultaneous α-tocopherol supplementation showed beneficial effects to all these alterations. Histopathological observations also showed hepatic degenerative changes after lead or hypoxia exposure either alone or in combination, but remarkable improvement has been noticed after α-tocopherol supplementation. Conclusion: Supplementation of α-tocopherol is beneficial to counter both lead acetate and hypoxia induced hepatic cytotoxicities possibly by reducing oxidative and nitrosative stress.
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